The involvement of expiratory termination in the vagally mediated facilitation of ventilatory CO2 responsiveness during hyperoxia.
In anaesthetized rabbits the influence of differential vagal cold blockade on the ventilatory response to inhaled CO2 during hyperoxia was investigated. Following total inactivation, the relationship between ventilation (V) and arterial PCO2 (PaCO2) was shifted to the left and steepened slightly over a range of modest hypercapnia, but was progressively flattened as hypercapnia intensified. The latter effect, suggestive of a vagally mediated facilitation of ventilatory CO2 responsiveness, was studied further. Differential vagal cold blockade to a temperature (5-11 degrees C) which abolished the Breuer-Hering inflation reflex (end-inspiratory tracheal occlusion no longer eliciting a prolongation of expiratory duration, TE) had no effect on V either during normocapnia or at a substantial level of hypercapnia. Only with further vagal cooling to 0 degrees C did the ventilatory depression during hypercapnia emerge, largely because TE failed to shorten in response to the hypercapnic stimulus. It is concluded that the integrity of expiratory-terminating mechanisms is crucial for the manifestation of the vagally mediated facilitation of V and its CO2 responsiveness which is evident during hyperoxic hypercapnia. A possible role is suggested for lung epithelial irritant receptors or for the tonic late-expiratory activity from pulmonary stretch receptors.
D000818:Animals; D001933:Brain Stem / Q000502:physiology; D002245:Carbon Dioxide / Q000494:pharmacology*; D008168:Lung / Q000294:innervation / Q000502:physiology*; D010100:Oxygen / Q000502:physiology; D011661:Pulmonary Stretch Receptors / Q000502:physiology; D011817:Rabbits; D012119:Respiration / Q000187:drug effects*; D014630:Vagus Nerve / Q000502:physiology*
D002245:Carbon Dioxide; D010100:Oxygen